Center for Advanced Imaging and Longevity

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Center for Advanced Imaging and Longevity

Center for Advanced Imaging and Longevity

@CAIALOfficial

At CAIAL—Center for Advanced Imaging & Longevity, we detect health issues early with high‑res imaging and screening, then guide your care for better health.

Beverly Hills, Calif Katılım Mayıs 2025
90 Takip Edilen170 Takipçiler
Ronald P. Karlsberg MD FACP FAHA FACC MSCCT |
Thank you for stepping up and addressing misinformation that directly harms patients and creates confusion. The solution is simple—ask for the data that supports the claims. We all need to push back and move the needle against this constant noise, much of which is driven by self-promotion rather than evidence.
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Center for Advanced Imaging and Longevity
This is an astounding fact and represents mainly just prejudice, ignoring the evidence base. It’s interesting: “never trust anyone who is selling something.” Isn’t that what you post? Many trusted you a lot. They bought your book. And you transparently promote it with comments outside of the evidence base? We think it’s time for you to take a second look at the data. You claim to be objective. It’s the only fair thing to do? Relook at the data, do a deep dive, and present a clear review of the topic that is fair and free of your prejudice.
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Eric Topol
Eric Topol@EricTopol·
@drjohnm I have been outspoken on the massive misuse of CAC testing for a long time (excerpt from my book in 2011) and have never ordered one.
Eric Topol tweet media
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John Mandrola, MD
John Mandrola, MD@drjohnm·
If only all these words were based on RCTs Meanwhile experts stay silent on the massive misuse of this test in the community
Khurram Nasir@khurramn1

One of the most meaningful evolutions in the 2026 ACC/AHA dyslipidemia guideline is the continued elevation of CAC as a central tool in preventive decision-making. We have come a long way. 1. In the 2013 guidelines, CAC was effectively sidelined. 2. By 2019, it re-emerged as a decision aid. 3. In 2026, it is now clearly embedded in the framework of risk assessment, treatment initiation, and treatment intensity. Two messages stand out. 1. First, CAC has become the preferred decision aid when treatment decisions are uncertain. This is not an uncommon situation. In real-world practice, uncertainty is the rule rather than the exception, especially in borderline or intermediate-risk individuals. #PowerOfZero provides a clear distinction who is and not at risk that for the decision whether lipid-lowering therapy should be initiated. 2. Second, the guideline goes beyond initiation. CAC is increasingly used to guide the intensity of therapy. Increasing plaque burden corresponds to progressively more aggressive LDL targets and therapeutic strategies. For example, individuals with CAC ≥300–1000 are recommended to pursue LDL reduction strategies approaching secondary prevention intensity, reflecting event rates comparable to treated ASCVD populations. This is a MAJOR shift. CAC is no longer simply a tie-breaker for statin decisions. It is evolving into a disease-guided framework for preventive intensity. From a practical standpoint, this matters.Risk equations estimate probability. CAC visualizes disease. 1. When uncertainty exists, seeing the burden of atherosclerosis often changes the conversation for both clinician and patient. 2. It also aligns therapy more closely with biology (GREATER DISEASE, MORE INTENSE THE TREATMENT) rather than risk-factor projections alone. IN 2026. CAC has moved from the margins of guidelines to the center of preventive cardiology. For clinicians, that represents one of the most practical advances in translating risk assessment into actionable care. Congrats @rblument1 @RonBlankstein @DrMichaelShapir & rest of the guideline authors @AJPCardio @ASPCardio @MichaelJBlaha @Sadeer_AlKindi @HMethodistCV

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JAMA Cardiology
JAMA Cardiology@JAMACardio·
In symptomatic patients without known coronary disease, #CCTA-derived plaque burden and volume independently predicted MACE beyond clinical risk and standard imaging findings. ja.ma/4l2k0jL
JAMA Cardiology tweet media
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Sriram Krishnan
Sriram Krishnan@sriramk·
On a personal note : I’m very proud of what we have done today in establishing what are going to be some very key issues and rules of the road for AI in America. This was a long process with many people involved that deserve credit ( including many who don’t always agree on everything ) and vigorous discussions but one I’m very glad we had.
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Center for Advanced Imaging and Longevity
Thank you for adding some evidence-based comments to this. It’s very important that the public recognizes the difference between social media posting and science. The single study is of course interesting and it has been presented in a fair manner, but let’s not overemphasize the treatment’s capabilities until it is fully studied and we know the long-term side effects. The drugs that are released—and that you’re referencing—have gone through more rigorous testing and yielded better results. Thank you for addressing this. @joerogan
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Ronald P. Karlsberg MD FACP FAHA FACC MSCCT |
Nattokinase is one of those therapies that catches your attention—not because of hype, but because there’s some real biologic signal. It clearly has fibrinolytic activity. You see effects on fibrinogen, PAI-1, and even small but consistent blood pressure reductions (~3–5 mmHg). That’s meaningful physiology. But when you stack it up against traditional therapy, the difference in evidence is hard to ignore: Statins → ~25–30% reduction in major events Antiplatelets → proven risk reduction in the right populations ACE/ARBs → outcome benefits beyond BP PCSK9 inhibitors → dramatic LDL lowering with hard outcomes Nattokinase hasn’t shown that. There are no large-scale trials demonstrating reductions in heart attack, stroke, or mortality. So where does that leave it? It’s not junk—but it’s also not ready for prime time. We don’t fully understand drug interactions, especially in patients already on antiplatelets or anticoagulants, and that matters. If you’re considering it, it’s a conversation to have with your physician—not something to layer in casually. There’s enough here to be interested. Not enough yet to rely on.
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Patrick Sullivan Jr.
Patrick Sullivan Jr.@realPatrickJr·
Joe Rogan recently discussed a study where 1,062 people took nattokinase for a year. Ultrasound results showed their arterial plaque actually shrank by 36%. This enzyme stops new blockages AND helps reverse the ones you already have. Let's look at the data and dosing: (1/12)
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Center for Advanced Imaging and Longevity
Look out for false claims about low cholesterol: The claim that “low cholesterol causes dementia” gets the direction wrong. When cholesterol is measured in midlife, higher levels are consistently linked to roughly a 2-fold increase in Alzheimer’s risk.[1] Genetic analyses support that this relationship is likely causal, not just associative.[2] So why do some studies show low cholesterol in people with dementia? Reverse causation. Cholesterol often falls in the years before diagnosis due to weight loss and metabolic changes driven by the disease itself. If you measure lipids late in life, you risk mistaking an early marker of neurodegeneration for a cause.[3][4] The argument that lowering LDL harms the brain also doesn’t hold up in randomized data. Large trials and systematic reviews involving tens of thousands of participants show no increase in cognitive decline or incident dementia with statins, even at very low LDL levels.[5] Major cardiovascular and stroke guidelines explicitly state that managing vascular risk—including hyperlipidemia—is part of protecting long-term brain health.[6] Once you separate midlife exposure from late-life decline, the pattern is clear: Elevated midlife cholesterol increases dementia risk. Lowering it does not cause dementia.
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Dr. Filippo Cademartiri
Dr. Filippo Cademartiri@FCademartiri·
🫀 Coronary Artery Calcium Scoring: Time for a New Standard? (Part I) Coronary artery calcium (CAC) scoring is a cornerstone of cardiovascular risk stratification. It guides statin decisions, aspirin allocation, and even de-escalation of therapy when CAC = 0. But here’s the problem: 📉 The current standard (120 kVp, 3 mm slices) hasn’t changed since 2007 — and reproducibility is limited. Small variations in positioning can reclassify patients. A new phantom study in European Radiology tested whether Photon-Counting CT (PCCT) can do better . 🔬 What they did: Scanned a calcium phantom under multiple protocols Compared tube voltage, slice thickness, radiation dose, and iterative reconstruction Benchmarked against modern energy-integrating CT (EID-CT) systems ⚡ Key findings: Thin slices (1 mm) at 120 kVp + 75% dose + IR2 dramatically improved reproducibility Agatston variability ↓ 37% vs standard PCCT ↓ 76% vs standard EID-CT Better detection of small and low-density calcifications Volume and mass measurements closer to physical truth All without exceeding noise thresholds 📌 Important nuance: Lowering kVp to 90 increased variability. PCCT benefits are not automatic — protocol optimization matters. 💡 Why this matters clinically: The difference between CAC 0 and CAC 1–10 changes management. Improved reproducibility reduces risk misclassification. Better detection of subtle plaques refines preventive decisions. PCCT isn’t just higher resolution. It may be the technical foundation for a new CAC standard. Now the real question: Are we ready to update a 20-year-old scoring paradigm?
Dr. Filippo Cademartiri tweet media
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Ronald P. Karlsberg MD FACP FAHA FACC MSCCT |
This isn’t just another incremental tech story — it’s a meaningful step toward dismantling the most silent, lethal disease we face: coronary artery disease. If a single-lead device in someone’s pocket can detect the electrical signature of an old myocardial infarction, we’re no longer dependent on chance findings or late presentations to uncover damage that’s already been done. Quiet detection like this is how we start shifting the balance — finding disease earlier, intervening sooner, and steadily reducing the toll of a condition that has hidden in plain sight for far too long. #Cardiology @vkhosla @DrMarthaGulati
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Chamath Palihapitiya
Chamath Palihapitiya@chamath·
Here is a cold email I got from Russell Straub last night about 8090. I asked him if I could share it. Who is Russell Straub? He’s a version of many of us: entrepreneur, more than 25 years in business, a capable team, looking for a way for himself and his team to grow through AI. If 8090 can help businesses like Russell’s thrive through the AI transition, we can help many millions of employers and employees and it will have been time well spent. “Chamath! After hearing you talk about it for many months, I was intensely curious to see if 8090 could be the platform to enable our small dev team of seven to 10X themselves! I personally had not coded anything since the late 1990's, but created my account Sunday morning and dove in! Instead of trying to pilot a project from our dev queue, I decided to start with a blank slate. I had a very basic document outlining the concept for a mobile app that one of my co-founders drafted in 2017, but we never had the time or bandwidth to pursue.  I think I just copied and pasted the 6 pages of text into the starting prompt.... 8090 attacked it aggressively, peppering me with questions and suggestions and very rapidly the Refinery cranked out an impressive set of requirement docs. I was impatient, so quickly moved to the Foundry where I continued to crank out blueprints! Then to the Planner where I was initially deflated when it asked me about my dev team and I sheepishly responded that I was hoping to use an AI agent to do the actual coding, but was quickly relieved when it responded with enthusiasm and suggested I use Cursor and GitHub. So...away I went!  (I had never used Cursor or GitHub but created accounts and had them up and running on my MacBook within minutes!) It was thrilling to see components come to life super fast... I just kept plowing ahead, everytime 8090 stumped me with a question I didn't even understand, I would just ask what it suggested - and it would give me a plain english recommendation - I'd approve it - and away we went! Anyway - I was so energized I corralled 5 of 7 dev team members for a zoom call at 11:30 am to walk them thru the capability.... Bluntly told them that my perspective as an outsider to the dev team was that we had 2 bottlenecks - one at the front of the team where the creation of requirements and wireframes are painfully slow and the backend of testing/QA/deployment.  (coding itself is probably infinitely fast and NOT the bottleneck). Lots of pushback on concerns about getting the platform "familiar" with our entire codebase, and the shortcomings of creating accurate GUI or wire frames.... BUT - my strong suggestion was for at a minimum for our primary requirements writer to dive in and give it a try - and be amazed! I've been a broken record for over a year saying that "AI is definitely going to make our business model obsolete - I just hope it's not this week!"  Our business is 26.5 years old.  I'm still amazed and thankful and grateful we've made it this far. I still think we have an incredible opportunity right in front of us to take advantage of AI to transform our business and transform our marketspace and maybe become a leader or THE leader! Every day is pretty dang exciting!” Try it here: 8090.ai
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